Changes

*High-throughput screen of anesthetics (and anesthetic reversal agents) in C.elegans. I could work in parallel in a different organism (e.g. yeast, jellyfish, hydra, sea anemones, corral, bacteria, plants, neuronal explants).

*High-throughput screen of anesthetics (and anesthetic reversal agents) in C.elegans. I could work in parallel in a different organism (e.g. yeast, jellyfish, hydra, sea anemones, corral, bacteria, plants, neuronal explants).

*Based on 30 years of in vitro studies (n>300), most anesthetics exhibit similar potency across a range of receptors. Most receptors are non-selective for ligands. What this paper addresses but doesn't answer is whether the receptors are present at the correct locations and necessary to the anesthetic behavioral response.

*Based on 30 years of in vitro studies (n>300), most anesthetics exhibit similar potency across a range of receptors. Most receptors are non-selective for ligands. What this paper addresses but doesn't answer is whether the receptors are present at the correct locations and necessary to the anesthetic behavioral response.

*Some anesthetics ('''ketamine, dexmedetomidine, etomidate, benzos''') are fairly selective, but are rarely used as sole anesthetics.

*Some anesthetics ('''ketamine, dexmedetomidine, etomidate, benzos''') are fairly selective, but are rarely used as sole anesthetics. Below, I list each of the ''in vitro'' binding affinities of these "selective" anesthetics, up until there is a change of one order of magnitude or greater for the next receptor.

**Ketamine binds to α4β4 nAChR w/ IC₅₀ of 0.144 uM, but has an IC₅₀ for the GluN1/N2C NMDAR of 0.338 uM.

**Ketamine binds to α4β4 nAChR w/ IC₅₀ of 0.144 uM, but has an IC₅₀ for the GluN1/N2C NMDAR of 0.338 uM.

**Dexmedetomidine binds to α_2A AR w/ K_D of 0.0014 uM and the M₃ mAChR w/ IC₅₀ of 0.001 uM.

**Dexmedetomidine binds to α_2A AR w/ K_D of 0.0014 uM and the M₃ mAChR w/ IC₅₀ of 0.001 uM.